CO2, Oxygen, the Biological Roots of Stress w/ Brad Marshall, Lewis Coleman MD, Steve Scott
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The brain is the tissue that consumes oxygen faster and more and requires it more than any other tissue by far. So if you do this to a grandpa, he comes out of the adventure with dementia. Dear God. Yeah. Well, you know, he belongs to God at that point. Wow.

A neighbor's choice.

Well, we're here in treat for a treat today. We've got my big fat gas panel today. It's because we're talking about hypoxia, oxygen, carbon dioxide, and the role that all of this balance between oxygen and carbon dioxide is something I've been fascinated with ever since Dr. Ray Peet got me interested in the topic. And along the way, these are some of my friends that are talking about these various issues

related to hypoxia and how to, you know, Brad focuses, Brad Marshall, our guest here, he focuses on the role of PUFAs, polyunsaturated fatty acids, also found primarily in seed oils and other industrial fats that are rancid and toxic. And he's focusing on how that affects the levels of hypoxia in our bodies. We can get into that at a deeper level with him. We have Steve Scott, who's the founder of Carbogenetics.com.

where he's using CO2 therapy, whether it's in the form of inhaling it or through the process of absorbing it through the body suit. I've enjoyed both methods and can attest that they are quite relaxing, and I think they're in store for a lot of transformative health effects for myself and improvements. Some world-class, world-champion athletes use his devices for CO2 and have amazing ecstatic victories.

Then we have the illustrious Dr. Lewis Coleman, who is the author of 50 Years Lost in Medical Advance, and also someone who is quite published, having completed the work of Hans Selye's The Quest for the Mammalian Stress Mechanism. He's an anesthesiologist and someone that we enjoy hearing from. So thank you all for coming on the program. Thanks for having us. Yeah. Yeah.

Now, Steve, are you doing the bodysuit right now or because you look really tranquil? I am not doing it now. I thought you had a sleeker black unit that I didn't know about yet. My goodness. Well, Dr. Lewis Colbert, you know, let's start off with you since you're our doctor in the house. You know, why do we need to understand oxygen and carbon dioxide and how that affects so many of the diseases that we have today, right?

Can you give us a little lay of the land of that? Sure. Well, the main focus of this would be what you call the mechanism of oxygen transport and delivery, which captures oxygen.

from the atmosphere and transports it to cells deep within the body because obviously every cell in the body rears oxygen for its metabolism. The main metabolic pathway of all eukaryotic cells that make up all your multicellular animals and plants that live on the surface at least of the earth use what

what's called the Krebs cycle as its main metabolic pathway. And I'm sure Brad has, has a lot to add to this, but I'm kind of interested to see what he has to say about the cellular metabolic pathways that I'm not an expert on, but I do know from my basic biology in college that the Krebs cycle is the primary pathogen

metabolic pathway that generates what you call ATP or adenosine triphosphate. Think of that as like little

cans of gasoline or oil that float around in your blood and your tissues. And the cells use that to power all their activities. It's kind of, I call it the universal, what do I call it? The universal source of cell and extracellular enzyme energy. So now the

The mechanism of oxygen transport and delivery is amazing. It's amazingly misunderstood and it's not taught properly. And this is an accident, in my opinion. It's actually been known for more than 100 years. It was discovered and characterized around the turn of the previous century.

where they studied how hemoglobin binds to oxygen. They call it the hemoglobin-oxygen dissociation curve. And I'm blanking. I'm trying to think of the name of the Danish researcher who was famous for this. But the important thing to understand is that— Is it Bohr?

Who? Bohr is his last name? Yeah, Bohr. Was it Niels Bohr? I can't think of his first name. Yeah. There's another Bohr who came along later who was prominent in theory. This Bohr was famous in his own time. He discovered this oxygen hemoglobin dissociation curve.

And that you need to understand that to understand how the oxygen transport mechanism works. So hemoglobin binds avidly to oxygen. It doesn't want to let go. And so when blood is passing through the lungs, hemoglobin,

the purpose of breathing is misunderstood. Everybody thinks that the purpose of breathing is to first and foremost bring fresh air into the lungs, which of course it does, and then get rid of carbon dioxide, which it does because oxygen has, I mean, carbon dioxide has been vilified as toxic waste like urine. So the idea is that you got to get rid of it all the time.

Actually, what's going on is carbon dioxide interferes with the binding of oxygen to the hemoglobin molecule. So what's going on here primarily is when you breathe, you're lowering the level of carbon dioxide in the lungs so that that oxygen

exaggerates the binding of oxygen to the hemoglobin molecule as blood passes through the lungs. And, you know, this is sort of, you can think of it as a safety reserve or something that makes sure that oxygen or that hemoglobin is 100% saturated as it passes through the lungs. Now, each hemoglobin molecule has four molecules.

binding sites. And the truth of the matter is that in a, anybody who's halfway healthy, or even when you're sick, your hemoglobin emerges from the lungs, a hundred percent saturated with oxygen. In other words, it binds to oxygen so avidly that it's not a problem saturating hemoglobin with oxygen.

And the first lesson here that nobody understands, doctors, nurses, you name it, you don't need to breathe oxygen. You know, the first thing they do when you get in a near ambulance or a hospital or any kind of medical personnel, they grab you and whack. They slap a mask on your face and give you 100% oxygen. It does no good. It's ridiculous. It's like a joke because oxygen

If you just breathe God's air, you're going to saturate your hemoglobin with 100% with oxygen. And the hemoglobin carries 99% of the oxygen in blood. And less than 1%, I think, however, I'm rusty on this, but a very tiny portion of the oxygen in blood is dissolved plasma. But it's insignificant. It's meaningless.

So already you see one of the fallacies of medical practice is this mania for making everybody breathe 100% oxygen. Well, actually it's harmful because...

Oxygen is extremely reactive. It's toxic. And if you say there's baboon studies, as we know best, if you have the baboon breathe 100% oxygen for more than 24 hours or so,

You can actually kill it. You know, it'll burn, literally burn the lung tissue. So this is not good for you. And furthermore, it's a fire hazard. Anytime you start horsing around with oxygen and a mask in your, you know, everybody, I mean, the nurses are just stubborn as can be. They will not listen to you. They'll get mad at you. Hey, you know, take the oxygen.

oxygen off or turn it down, they'll get it up to 10 liters or something. And the oxygen is flying all over the place. And so you get these oxygen fires in the hospitals. And I mean, they really hurt people. It's funny. And they don't understand that it's not serving any purpose whatsoever.

Okay. So then the heart pumps blood, you know, from the lungs. It goes to the left side of the heart. And the left side of the heart, of course, is a lot bigger and stronger than the right side of the heart. And it pumps blood out.

to the rest of the body. Now here comes the next misunderstanding about this mechanism. Everybody thinks that blood pressure is the driving force of blood flow. No, they think that blood flow characteristics are identical water, but water and blood are profoundly different. Water is what you call a Newtonian fluid.

What that means is when you accelerate water in a pipe or an artery, it causes exponential increases in blood turbulence and turbulent flow resistance. And the faster you accelerate the water in the pipe or the artery, the greater the flow resistance that it exerts. It forms these turbulent flow patterns.

patterns with the forward moves along the inner wall of the pipe. And those curve around and they push the slower moving elements of the water to the center of the pipe. And then it goes backwards. And the harder you push, the more

You know, flow resistance you get. That's why it takes so long to fill a swimming pool or even a bathtub. You can only put so much water pressure on a municipal water system. And if you get beat, the turbulence becomes a practical problem. I hope I'm making myself clear.

Um, so blood contains particulates, namely the red blood cells, which are unique in vertebrates. I mean, all vertebrates have red blood cells. The hemoglobin is always enclosed in a cell, a red blood cell. And, you know, like birds have, um, um,

a certain shape and size and buoyancy to their red blood cells. It's different from amphibians and arars, or what you would think of as crocodiles. Every different class of vertebrates has a different type of blood cell. They can be identified by their blood cells. So the red cells of mammals are tiny, way smaller than the blood cells of any other mammal.

or any other vertebra, I'm sorry. And they're biconcave. They call them scaphoid. So when blood is accelerated in an artery, then all the cells spontaneously form what we call stacks. You know, they form little, you know, towers or stacks. The French call this rouleaux.

And so those stacks, as they form, they prevent the formation of these turbulent flow patterns. And by the way, this used to be misunderstood until about 20 years ago. And a team of Belgian engineers used laser photography to photograph water flow in pipes.

And they literally took laser photographs to prove this, you know, computer derived theory, mathematical projection of flow turbulence. And so they confirmed, they tested and confirmed the theory. The head researcher's name was Hoff, H-O-F. And if you want to read a really interesting engineering study, I recommend that. It's really an eye opener.

So when the heart beats...

it expels its contents in less than a tenth of a second. It's really amazing. Nobody appreciates this. It just goes, boop, that's it. And the rest of the time, you know, it beats, you know, a minute or depending on your health status and so forth. And like a trained athlete, it'll have a resting heart rate below 40 beats per minute. It's

his heart is so efficient. He's got so many capillaries, his flow resistance is negligible. And so his heart just goes, eh, you know, eh. And when he exercises his heart rate right up to 80, maybe, you know, while he's running 90 miles an hour, uh, because he he's, he's got exercise conditioning. He's formed extra capillaries in his muscles and tissues, uh,

So there's virtually, you know, the faster he runs and the harder he exercises or whatever, this recruits more capillaries and the flow resistance doesn't increase. And your blood flow in your arteries is like superconductivity. It's like the harder the heart pushes the blood, the lower the flow resistance becomes because the red cells, am I making myself clear so far? Mm-hmm.

Okay. All right. If you guys have questions, you know, squeak. All right. And I'll try. Brad, what are you thinking? How would you like to chime into this so far? I mean, I'm just curious to hear the rest. Most of what I focus on is what happens once the oxygen is delivered to the cell. So I haven't thought as much about these components of it. So I'm...

Right. Yeah, I was looking forward to hearing what you had to say, but I'm glad to get a chance to paint this picture because it's not your fault. They don't teach this in medical school. Now, they did in my medical school. Let me just make it here.

They taught it in my medical school, but I think that my medical school was exceptional, really. I was very fortunate to go there, but at a great rate to go on and complete the picture. So the blood is expelled into the arterial tree. Now, here again, everybody in conventional orthodox medicine

again, they're assuming that blood pressure is the driving force. So they think that blood flow is controlled by vasoconstriction and vasodilation, but blood is a non-Newtonian fluid. So when you have narrowing of an artery, all that happens is you speed up the blood flow.

So if an artery contracts, then the blood speeds up. And well, once in a while in the operating room, if you're in there for a long time like I was, 40 years or whatever, once in a while, a surgeon makes a mistake and goes, oops, and it slices an artery. And you'll see the blood go zip, zip, zip, right?

Because the artery is trying to contract and it speeds the blood up and then it squirts quite a distance, right? It's got a, you know, it accelerates it by velocity. And of course your simplistic thinking is, oh, well, obviously the heart beats and propels the blood and that seems obvious, right? But real hemodynamic physiology is,

backwards from what our common sense tells us. Everything is different. Everything is backwards. So what happens is that when your heart expels this bolus of blood out into the arterial tree, it's muscular, but it's also elastic.

And the muscular muscle is different from the other muscles in the body, like the cardiac muscle has lots and lots of mitochondria in it because it's all the time working.

The skeletal muscles are sort of midway in between. They have a fair number of mitochondria, but that, you know, produce the ATP energy. And Brad will get into telling us all about that, I'm hoping. And then...

The vascular muscle has very few mitochondria because it's absorbing its oxygen straight from the arterial blood, which is 100% saturated with oxygen. And it doesn't work very hard. So what happens is the entire vascular tree gently expands to accommodate the bolus of blood that's injected into it by the heart.

And it functions as a secondary heart. So the heart's not doing all this work by itself. So now as soon as the heart has expelled its contents, now everybody thinks that everything in the body is super, super efficient. But muscle isn't. Because when muscle contracts, it's like a...

a ratchet system where you have actin and myosin moving vis-a-vis each other through little catches or ratchets. And it goes click, click, click, click, click, click, click, click, click, like this. And each of those clicks consumes ATP.

But then it can't let go unless it has to unclick. And each unclick takes another ATP. Clunk, clunk, clunk, clunk, clunk, clunk, clunk, right? So now the heart itself...

beating a lot. It works all through lifetime, right? But it's weak. It doesn't have to work very hard if you're healthy, the Newtonian characteristic of blood. In other words, the harder it beats, the easier it gets to squirt the blood out of itself. Okay. So, but then the heart has a cartilaginous skeletal framework so that when it relaxes,

the the cartilage opens up the uh heart or restores the heart's volume you know volume and pulls fresh blood from the atria into the ventricle all at once without the heart having to consume a lot of extra energy uh relaxing itself okay so um

Anyway, so now the arterial tree, having been charged with a bolus of blood, it very gradually and gently restores itself to its resting volume. As it does so, it pushes the blood towards the capillary beds. Well, now what are we measuring when we measure blood pressure? Okay, well, here's what happens is the distal third of the aorta,

is about a third the diameter of the proximal aorta oh i'm running out of battery power on this darn thing uh that's what's squeaking let me switch i may have to switch to a different uh speaker and headphone here didn't expect this to be a problem uh i can i can jump in for a second um yeah why don't you why don't you chime in for a second and now and while i get this straightened out

Yeah, so as you were talking, you know, I'm an evolutionary, I think like an evolutionary biologist, right? I like to put things in order of sort of what came first. And what you're describing is very interesting because I know that, or I'm pretty sure that I know that when you look at the chordates, chordates are...

things that have a spine mostly um except for the oldest uh chordate is a thing called amphioxus which is a little um looks like a fish but it's not a fish it doesn't have a skeleton

And you can still catch these. They're in the shallow bays and they eat them in Japan. And anyway, what's interesting is the Amphioxus does not yet have a heart, but what it does have is contractile blood vessels to move. It's not really even blood yet, but it uses it to move the kind of interstitial fluid around through the organism. So what you're describing is,

is perfectly logical with how things kind of evolve. The contractile vessels or the contractile arteries came first and the heart came later probably as a way to help shunt the blood into the contractile arteries.

Yeah, what you're talking about is a different stress mechanism. And so all I'm talking about is exclusively the mammalian stress mechanism because each vertebra has a different stress mechanism.

I was just saying that in the chordates, which is things with backbones, animals, or mammals, lizards, fish. That's what we need more of in this country, don't we? People with some backbones. That's right. Bring back the chordates. Yeah. But the amphioxus, the lancelet, is at the base of that.

tree, that phylogeny. So they have a cord, they have a notochord, which is what eventually became the skeleton, right? Or the spine, but they have these contractile arteries, just as he was describing, and they do not yet have hearts, right? And so the contractile arteries came before the heart actually did, interestingly. And insects is another example. I mean, we're talking about different strains.

Every time we do a shift like this, you know, the cordyceps is one thing. They have their stress mechanism. Insects have another stress mechanism. So insects inhale air through their abdomen through sphericals. And so when they if you look at them carefully, though, you see their abdomen is expanding and contracting. And it's a very, very effective stress mechanism.

but probably is only good up to a certain size. And then you start running into size problems. Now, the only, what I've really done is I've identified the first stress mechanism to ever be described. And that really is courtesy of thousands and thousands of research studies that have been performed on

mammals because everybody's interested in medicine and the government subsidies pay for that. They don't pay for the biologists to do this kind of intense investigation.

And of course, then there's plant stress mechanisms too. You know, the big classes of plant gymnosperms and angiosperms that we see on the surface of the earth. That's the most common two categories. But then there's, I don't want to go too much further here because I'm out of my water. Real son could, you know, I'm trying to get him. He's going to get his PhD here and,

a couple of months and then I'm wanting him to, to see if he can describe one of the stress mechanisms for plants. But that's a different ball of wax. That's plants are way complicated. But anyway, to finish off what I, where I was because the blood,

By the time it gets to your capillaries, the flow is relatively constant and uniform. Your blood perfuses through the capillary beds and your cells are constantly generating carbon dioxide. The slightly higher level of carbon dioxide in your organs and tissues

loosens the binding of oxygen to the hemoglobin molecule and releases it into the tissues. Now, you know, I proved this in the operating room for myself, although there's plenty of other studies that have done it too. When, you know, like in the operating room, what I did was I gave the patient a lot of narcotic drugs.

And narcotics reduce respiratory drive. And so then the CO2 level within the body would build up. And the partial pressure of the carbon dioxide normally in the body is about 40 torr, okay, 40 PSI.

but I would let it go all the way up to well above 100, shall we say. I don't want to scare anybody, but it's totally harmless. Now, there's dog studies. The only way you can get in trouble with ecrinoxine is if it gets up well above 200 torr, at which point you're flirting with...

you know, the, uh, carbon dioxide will start to, um, interfere with the binding of oxygen in the lung. Okay. Because, uh, it inhibits the binding to the point that you start to, to, um, um,

you know, have your arterial bloods not saturated anymore. And I hope I'm making myself clear with this. I didn't get anywhere near that in the operating room. And besides, nowadays we have what you call pulse oximeters. Now this is a whole different lecture. It's not the way this thing works.

Have you guys all heard of a pulse oximeter? Know what I'm talking about? You all do? Yes, yes, yes. Okay. All right. Well, the pulse oximeter shines three different wavelengths of light on your skin and it bounces those wavelengths off the hemoglobin molecule and then it has a photonic receiver and then they have an algorithm

that analyzes relative reflectance of those three different wavelengths of light and tells you whether your hemoglobin is, is, uh, straighted or not. Well, it gets kind of complicated, but basically when the, um, when the, um, you know, the, the algorithm says that the, it's got 60% saturation, um,

it's the hemoglobin is is actually 100 saturated or or close to 100 saturated because what it's looking at also is the the oxygen saturated in the plasma so you know if you if you just run the um

patient with a pulse oximeter reading 60, he's fine, actually. But you can't tell that to a nurse. But what's going on there in the operating room, in 99.999% of the operating rooms throughout the world,

Anesthesiologists have been brainwashed to think that carbon dioxide is bad, and mechanical hyperventilation is the answer. Okay? You've got to breathe for that patient by God, and more breathing is better, no matter what. More, more, more. Okay? So they hyperventilate the daylights out of the patient. They deplete the carbon dioxide from the patient's body.

And the pulse oximeter is way happy because now you've exaggerated the binding of oxygen to the hemoglobin molecule. But on top of that, you've supersaturated the plasma. And the pulse oximeter goes, ooh, it runs right up to 100. And all your nurses go, wee, good doctor, good doctor, right?

But what's happening is that the body is depleted of carbon dioxide, so it's not releasing oxygen into the tissues. And now the brain is the tissue that consumes oxygen faster and more and requires it more than any other tissue by far. So you do this to a grandpa, he comes out of the adventure with dementia. Dear God.

Yeah, well, you know, he belongs to God at that point. And this happens all the time, and everybody goes, why is that? How come? It's a big mystery, don't you know? My God, we've understood this for more than 100 years. This is basic physiology. It's like they control medical education and textbooks and journals and medical boards and

And it's like the tail wagging the dog all over the place. So, you know, medical students are brainwashed. They don't even know it. And then you go into anesthesia school and you're brainwashed 10 times over. And you cannot change these people. Doctors are not scientists. They're doing this fundamental psychological work.

they got to be like everybody else. They want like lemmings jumping over a cliff or, you know, you know, penguins in a herd or a flock, you know, they're all, everybody wants to be all cozy and quacking alike. But Dr. Coleman, then not only do they cause dementia, they also give people diabetes when they go to the surgery practice, right? Yes. Well, yeah, because,

Let's see, how would that happen? Well, I hadn't ever been asked that question before. I can tell you that carbon dioxide not only loosens the binding of oxygen to hemoglobin and releases oxygen from the hemoglobin into blood, but it's the sole source of respiratory drive, you know, what makes you breathe, right?

and it directly releases nitric oxide from the vascular endothelium. Now, your capillaries have only one layer of cells, and that's pure vascular endothelium. And the vascular endothelium is this delicate layer, one cell thick, on the inner surface of all your larger blood vessels. So,

Actually, the vascular endothelium is the heart and soul and focus of the stress mechanism, the mammalian stress mechanism, which I won't go into right this moment. But carbon dioxide is the primary regulator of the capillary gate mechanism that operates in capillaries that regulates the flow resistance in your organs and tissues.

So carbon dioxide releases nitric oxide. Now, the nitric oxide binds to calcium, reduces thrombin activity, and I'll cut this whole thing, but in the research literature, this is called nitrurgic neurogenic vasodilation. Sorry, I have to say that because that's what it's called. But

It doesn't cause vasodilation, like opening up of the blood vessels or anything like that, like everybody thinks. Because everybody's got this stubborn, entrenched belief that the blood vessels muscularly contract and then relax. So they think this must be vasodilation, but it works at all. It's actually what's happening is you're generating...

a protein called insoluble fibrin in the capillaries that forms little strands and the strands are generated by sympathetic nervous activity and so they form in the capillaries and they increase flow resistance they don't close the capillary per se we we can speak of closing the capillary gate or opening the capillary gate but you're not literally

shutting off flow in the capillaries. You're just slowing it down. Okay. And then when you get rid of the insoluble fiber and it will spontaneously self-destruct because it contains a link in its molecular structure called plasminogen. And the plasminogen breaks down into an enzyme called plasma. Plasminogen.

that attacks the insoluble fibrin structure and disintegrates it into what you call fibrin split products, that opens the capillary gate. I'm making myself clear? Yeah. Brad, do you understand?

I mean, yes, I understand that. So this is the process that instead of the artery or the capillaries, I mean, physically constricting, instead it's adding material inside, which increases resistance to flow. There you go. Okay, good. Via mechanism entirely different than literal dilation and undilation. Okay, excellent. Don't the blood vessels higher up in the tree, don't they have smooth muscles that...

Yes, but like I said, even if they do contract, and you can make them contract with electricity or something like that and certain chemicals, but all these studies are done in vitro, outside the body. Okay, and they take a section of artery and they put it in a salt bath or something, and then they goose it with electricity, water.

or this and that and the other chemical. And yeah, it's muscle and the muscle contracts and the lumen gets smaller. That's all true. But in real life in the body, if you actually constrict the diameter of the blood vessel, what happens is it just speeds up the blood. Doesn't do any good.

Because normally when you like breathe carbon dioxide, there's been studies showing that it increases blood flow to the brain by 50% or it, and it was attribute that to vasodilation. You're saying it's actually vasoconstriction that's increasing the blood flow, blood velocity, blood volume. No, no, there's no vasoconstriction. There's no vasodilation going on, except that when the arterial tree is expanded by that bolus of blood,

Then it slowly contracts, and the muscles, you know, not very strong muscles. They can't do much work because they don't have any mitochondria. So, you know, they slowly – it slowly restores its resting volume, and that's not – it's like a very gentle force. I mean, it's –

I feel like we're talking about the same thing. It's just you're arguing that the mechanism by which the blood flow is increased or reduced is different than is commonly believed, right? Correct. Essentially, in principle, the constriction happens, but it's happening by a mechanism different than literal physical constriction. Right.

And I'm hoping I can persuade you to read my book and critique it because it's got a chapter in there on the unified theory of biology. And that's what I want. I've been looking for a biologist like you who can appreciate this and evaluate it for me.

I think just from what you've said, you're going to really enjoy reading this. It's going to give a radically different view of anatomy, taxonomy, behavior, speciation, evolution. It's going to resolve the disparities of Lamarck and Darwin and Baldwin and saltation.

Okay. These are all major mysteries, right? In biology. What's the name of the book? Sorry. Just so people know, this conference came together this afternoon, so we haven't had a lot of time to do background research. Oh, right. Yes, you said that. Yeah.

uh yeah i'll get you a a pdf copy of uh by email or i'll send you a link so you can get it download it from my dropbox sure if if that is adequate um

That should be fine, yeah. Brad Marshall's been looking into this concept of how oxygen relates to obesity and these hypoxic states that people are in when they're morbidly obese. And I wanted to bring Steve Scott on because he's into researching that.

uh co2 and its relationship to oxygen and healing you know people's problems with obesity and all kinds of other metabolic dysfunctions and i thought you guys could weigh in together so just jump in and talk about it i don't want to i don't want to get in the way yeah let's hear your idea let's steve have at it for a bit here yeah well i'll let brad go talk about his ideas about obesity and hypoxia and whatnot yeah okay

Well, so, right, so I look at the

I look at inside of the cell what's happening, right? And this is, in my opinion, this interview is actually very well-timed because I'm literally writing, my plan tomorrow morning is to write this article and post it on my blog. So probably that'll maybe be out before this is, I don't know, come out together. And the idea is that what I've seen is that once oxygen is actually delivered into the cell,

One of these other big misunderstandings, like you've mentioned, when you take biology 101, they show you this drawing of a cell and the cell has like a nucleus. And then around the nucleus is the endoplasmic reticulum. And over here, there's a big old mitochondria.

uh, that's not reality. The reality is the mitochondria are very small and they're embedded into the endoplasmic reticulum, which is all around the nucleus. Right. And so, so you have the nucleus and around that there's this, these layers of endoplasmic reticulum and there's layers of mitochondria buried in there. And so, um,

So once the oxygen gets into the cell, it now has to migrate through the endoplasmic reticulum to get to the mitochondria. Now we have a system of enzymes that

One is called delta-6 desaturase. There's a delta-5 desaturase. There's this delta-9 desaturase. There's cytochrome P450 enzymes, and there are cyclooxygenase enzymes. I might be wrong about the cyclooxygenase enzymes, but the other ones I'm sure of, they live in the endoplasmic reticulum.

And so when those when any of those enzymes are elevated, that predicts your likelihood of developing diabetes over time. That predicts your they're strongly correlated with, you know, degree of obesity, degree of metabolic syndrome. To me, that system looks like.

Those enzymes are there to prevent the oxygen from getting through the endoplasmic reticulum to the mitochondria. They're essentially an oxygen shield. And

Why does it work that way? Because when a bear wants to fatten up for winter, all they have to do is increase the expression of these desaturated enzymes. And that will fundamentally flip the adipose cell from being primarily oxidative to being primarily glycolytic.

Right. It's a it's a pseudo hypoxia. The problem is not always that. I mean, there are problems with oxygen delivery. It's not that they're not. But there's there's this further problem once the oxygen gets into the cell that if you're if you're desaturated enzyme system is cranked up.

that oxygen is essentially being intercepted as it moves through the endoplasmic reticulum. And the primary fuel of all these systems are, well, at least the delta-6 desaturase and the delta-5 desaturase in the cyclooxygenase system is linoleic acid. The cells prefer to put linoleic acid into the SN2 position of the

the membranes and the, the endoplasmic reticulum is a membrane, right? It's a membrane that lives inside of the cell. And so the endoplasmic reticulum is rife with linoleic acid. And the, and the role of it is when, when, you know, when the bear decides it needs to fatten up for winter, you've got the fuel right there along with these enzymes, Delta 60 saturates,

The linoleic acid, by the way, is constantly being released from the membranes and then being re-isolated in this cycle called the land cycle. And

And so the cells take the linoleic acid, delta-6 desaturates, puts a double bond in it. That consumes a molecule of oxygen. Then another molecule sticks an acetyl-CoA group on it, and another enzyme, D5D, desaturates it a second time. That consumes another molecule of oxygen. And then a cytochrome P450 enzyme,

sticks another oxygen on the end, making it 20 heat at that point, right? And that consumes a third molecule of oxygen. And now the 20 heat is exported via transporters in the cell into the blood

And it's transported and it can be burned to the mitochondria or it can be urinated out. But the point is that that linoleic acid was essentially used as a fermentation process to soak up the incoming oxygen so that it's not getting to the mitochondria and exported from the cell. That is my hypothesis of how the system works and why these desaturase enzymes exist.

are elevated in um in in if you know if winter is coming and hibernating animals and they're elevated in obesity and diabetes i believe that is that is that a purposeful thing or is that just a result of having too much linoleic acid or something like that or is it it's intentional like

So it's so I think it's a lot of things, you know, it's I think that it's I think having a lot of linoleic acid is, of course, providing fuel for the system. Right. What you actually see and this this. Right. So one of the paradoxes that we see is that, you know,

So a lot of us think that we've been consuming too much linoleic acid and linoleic acid levels have increased over time. Right. So you're providing more fuel for the system. However, if you look at population level studies, if you assume that everyone is eating the same amount of linoleic acid on average in the U.S. population, which is probably more or less true, right.

The ones who have the lowest level of linoleic acid in their adipose tissues are actually the most likely to develop diabetes.

And some of this obesity. And so I think what's happening is that in those people, your adipose, because remember, once this 20 heat is produced and ejected from the cell, that cell can just replace it from linoleic acid in the bloodstream, free fatty acids, right? The adipose tissues are constantly releasing these free fatty acids and the adipose tissue can constantly take them up, suck them into their endoplasmic.

uh reticulum membranes and use them as part of this ferment i call an oxidative fermentation right and so now your adipose tissues instead of being oxidative and and using their mitochondria to do oxidative phosphorylation now they're fundamentally glycolytic and and the fuel for them to remain glycolytic is is is the linoleic acid however all of this is controlled by enzymes

And so if you don't have elevated delta-6 desaturase, delta-9 desaturase, and delta-5 desaturase, you won't necessarily have this problem. And in my opinion, that explains why different genetics are more prone to different – there are known –

polymorphisms in these genes that make them more or less active. And if you have the active version of Delta 60 Sats race, that predicts that you will be more likely to become obese and or diabetic. And so I think that's, you know, that's just controlling this process of fermentation. And then just to, just to bring that method home, when you look in a,

When you look at an obese person, they put catheters into the capillary beds. You can see that the fat cells are not using... They're using very little oxygen. And in fact...

compared to the rest of the body, right around the adipose tissue is actually higher in dissolved oxygen than the rest of the body. So the oxygen is getting there, but it's not getting in, at least in the adipose tissue. Now that situation might be very different in muscle and in liver, but specifically in the adipose tissue, the adipose use these enzymes, I believe, to become hypoxic. And so you have this irony in the

there's an enzyme called um hif-1 which is an uh an oxygen sensor um that's in all the cells and when ox when cells become hypoxic hif-1 is or the enzymes that are controlled by the transcription factor hif-1 are increased that tells you that the hif-1 has been activated and um and in obese tissues you see this ironic situation where the tish the the uh

oxygen pressure in the tissue is not necessarily bad, but yet the oxygen or the cells have this activated HIF-1, a sign of hypoxia. It's a pseudo hypoxia because the oxygen is there, but it can't get to the mitochondria and therefore the cell is actually in oxygen stress. I do have a question. Sure. Not to interrupt you, but I've been wanting to ask this question

I mean, this is very interesting what you're saying. When I was in medical school, which is like, I'm a dinosaur, right? But I remember they taught us that there's three essential fatty acids.

in your diet, linoleic, linoleic and arachidonic acid. And they didn't have any idea like what you're talking about back then. I mean, you're, you're, you know, got all these modern studies with newer research techniques and everything. But what, what, what about the linoleic and arachidonic acids? What are they doing?

Well, so it's kind of the same, especially that I think the two that are most responsible for this are the linoleic and the linoleic acids. Both of those are in a position where they can consume the most oxygen in the, because to go from the process of going from linoleic to arachidonic acid consumes two molecules of oxygen. Can they be converted back and forth?

Yes. So the, the, that's right. Right. So after Delta six D and Delta five D six D and D five D act. Now it's arachidonic acid. Arachidonic acid is the thing that yet another oxygen is used to convert it to 20 feet. And that's the thing that gets eliminated in the urine or, or can go into the mitochondria as well. I don't think they knew that back, back in my day. Well, I think they, I mean, I think they've,

They may not have known that. I think, yeah, I don't know when the dynamics of those enzymes were figured out. Probably later. But I think it's only, well, I guess it's only sort of put together that

The idea that this system is essentially acting as an oxygen chip. You know, everybody looks at... It's similar to what you're talking about, where, like, we see all the clues, but you're looking at the problem wrong, right? What we see is we see all these... People say, oh, it's these oxidized... It's these oxidized lipids that are causing all of these problems. It's the 20 heat that's causing... We see the 20 heat rise, and it's elevated in obesity. The 20 heat is causing the problem. I'm saying that the 20 heat is...

just a symptom of the problem. The problem is the fact that these enzymes are consuming oxygen in the endoplasmic reticulum and not allowing it into the mitochondria. And evolutionarily, and evolutionarily for mammals,

This is an advantage because if you live in a northern climate where, you know, you need to hibernate half of the year, then then this is a really useful system. Right. And so and so when I go and so this is a good analogy and why I think about evolution. Right. So in my current blog series, I talk about copepots.

copepods are like tiny shrimp they're little crustaceans and they live in the ocean they're basically the the basis of the marine food web and they eat algae and they in turn get eaten by like bait fish right and so um

And when you look at the copepod, what they do is they – if you feed them a type of algae that has linoleic acid and linoleic acid, they just vaporize that. And they'll hang on to some of the – like the DHA and the EPA, the longer chain omega-6 and 3 fatty acids. But –

the linoleic acid and the linoleic acid go just like that. And, and furthermore, what they do is very interesting is the female copepods when they're very, when they're actively producing eggs and they're very anabolic, they swim up to the surface during the day or sometimes,

or sorry, during the evening, they feast on algae and then they swim back down to the oxygen minimum zone where dissolved oxygen is very low. And my argument is that this makes them very anabolic and glycolytic and that they're using that linoleic acid and the linoleic acid

as the fuel for this oxidative fermentation, whatever oxygen is there, they're using for this fermentation and that actually clears NADH from the cell and it allows them to continue to do glycolysis because we have this longstanding problem in all cells that when you do glycolysis, when you use glucose for fuel, you create NADH.

And NAD takes a pair of electrons from glucose or from the glucose byproducts. And now those electrons have to go somewhere.

And so a lot of things have solved this by fermenting the pyruvate created from glycolysis back to lactate and they spit out the lactate. And that's how you make sauerkraut, right? The bugs in the sauerkraut are taking glucose out of the sauerkraut. They're doing glycolysis to generate ATP. Then they're ejecting the carbon framework of that glucose.

as lactic acid and the sauerkraut becomes acidic. And other animals have solved this through fermenting alcohol, such as yeast. But

In a multi-celled animal, you need a different solution, right? You can't, all of the cells can't be ejecting lactic acid into the interstitial fluids or you're going to die of lactic acidosis. Similar argument for ethanol, right? And butyrate isn't great to do that with either. And so they had, so the animals had to come up as they became multicellular, had to come up with a solution to this problem, right?

And I believe their solution was ferment the PUFA. That's the thing that you can ferment and eject and you won't die of acute toxicity. Right. And so and the sort of evidence of this is if you look in the medical journals, they say, well, 20 heat is an important factor.

signaling molecule that's used for angiogenesis which is uh when cells want to build more capillaries um and of course that's true of course that's true but uh the copepods are also fermenting the linoleic acid and the linoleic acid and they're making these oxidized lipids and they don't have blood vessels yet right and so that system predates blood vessels and so that that

role of these uh oxylipins signaling and stimulating blood vessel growth clearly came later right the the the oxidative fermentation is the fundamental underlying process that was their first uh the the animals the clever animals as i like to say on the blog use that as a signal oh we need oxygen here we need to introduce blood vessels but i believe that happened probably you know 100 million years later hundreds of million years later um

I'm going to really, I mean, I hope that we can have an ongoing dialogue because you obviously know way, way more about intracellular metabolic pathways than I do. I mean, this is all new to me. Fascinating. I remember I blundered into a chart once.

that indicated that you guys, you know, the researchers have identified hundreds of metabolic pathways inside the cells. And my take is that there's these athletes who are involved in extreme exercise conditioning, like cyclists, like Lance Ams,

What? Armstrong. And I forget, there was a guy, an American before him who was kind of famous as the first American to win that big bicycle race in France. Yeah. And Greg Lamont. Now, Greg Lamont, apparently, this was in Scientific American many years ago. Apparently, he over-exercised and...

burned out his mitochondria and he had to quit competing. And so he actually had a muscle biopsy taken and they've discovered that his cellular mitochondrial level was abnormally low. And so he just had to retire.

um lance armstrong was also the subject of a scientific american article this is when i was in high school okay this is ancient stuff um i mean the guy was a real serious athlete and so he was participating with researchers to study exercise conditioning and um you know he he was just way into it i mean he he didn't

win these races just by cheating. You know, he was really, really well conditioned. Anyway, there's, I mean, we could go at this for a long time, but. I want to add something to this here. Yeah. So how, how do you, how does that line up with your, you know,

your view of the stress states like obesity and cancer and these other states and relationship to these gases like oxygen and carbon. Sure. You talked about to me that you could potentially treat something like obesity with just

just giving people CO2 every night when they're sleeping, you know? So why, how would that work? What's the mechanism without, you know, going too deep into it, but just briefly. Well, obesity is a disease unto itself from the point of view of stress theory. I think what's going on is that as you become so heavy and

that interferes with capillary flow in your tissues because, you know, the tissues are just like I know. And certainly in the case of the chest, the weight of the fat on the chest wall presses down and interferes with blood flow actually going through the lungs.

Now, I don't know enough about the intracellular biology to talk intelligently about that. This is what I like. I like to combine different fields of interest and see what happens. Oh, yeah. This is really good because this is where you tend to start to get serious questions.

insights or epiphanies you know by going into other people's fields and then you've discovered relationships like this so i think that that you know i'm i'm really tickled pink by meeting brad i mean it's yeah i mean what i always say is that um biology is feedback loops fighting feedback loops yes right and so what we're talking about is a positive feedback loop that that that

Right. The the cells are glycolytic. The fat, the fat cells start to expand. That puts pressure on the capillaries that reduces blood flow even more. That causes the adipocytes to become even more glycolytic and the system becomes self-reinforcing because. Yes, yes, yes, yes. And that is what.

And that's what controls the state, right? The state of the organism. What state are we in? Are we an organism that fundamentally believes that winter is right around the corner and we should be conserving fuel? Or are we fundamentally an animal that believes that it lives in the tropics in eternal sunshine and there's no need to do that? Right. Right. And so far as just my work on this mammalian stress mechanism goes,

I'm particularly excited right now because when I wrote the book, the one great, you know, question mark I had was what causes chronic illnesses. I have the stress mechanism provides a very simple, straightforward explanation of cancer and critical illness and diabetes, by the way, type one and type two. But actually, yeah,

What I knew at the time of writing the book was that amyloidosis seemed to be the cause of type 1 and type 2 diabetes. Because it turns out, when I did further work after I finished publishing the book, I mean, I just keep learning more and more. But I did a review finally of, I just started looking at like,

all you have all these different diseases that are supposedly unrelated to one another right that's that's your orthodox medical theory is that all the diseases are unique none of them are related to any of the others right stress theory is saying no it's hyperactivity of this one that's causing all these seemingly different diseases

And after you've read the book, you'll understand this better, how a single mechanism can actually do that. Okay. I mean... Yeah, I mean, that's very much in line with my thinking. Yeah. Essentially one fundamental underlying process. Right. And that's where we need to have an ongoing conversation here. But since I published the book...

I had this, what to me is like a breakthrough. I'm pretty excited about this. I didn't understand what caused chronic illnesses, all these rheumatoid diseases. Nowadays, orthodox medicine has come to classify diseases

between atherosclerosis, diabetes type 1 and type 2, and hypertension, essential hypertension as chronic illnesses or rheumatoid diseases. Okay. Now, a lot of people want to

pin everything, pin their tail on the donkey of the immune mechanism and say, well, it's autoimmune disease and it's the immune mechanism is attacking the body in some way or other. There's no convincing evidence to support that idea. I 100% agree with you. Yeah, but everybody wants to hang their hat on it or pin their donkey tail on it. And

I'm actually writing a paper right now. And so when you read my book, I want you to bear in mind that there's another great... It's like, you know, when I was in school, they talked about the plants and the...

But now they're looking at the fungi. And then they're also looking at the archaea cells, right? Those were completely unknown. And the fungi are now appreciated as like the third great kingdom.

Kingdom, there you go. I mean, I had a taxonomy class at Ohio State. The mushroom kingdom is rising. Yes, it's going to get us. Here in Bakersfield, you know, it's serious because you get coccidioidomycosis. And, you know, if you get around an ocean site on a windy day, a friend of mine got this, it damn near killed him.

And it's really, really dangerous. Dr. Coleman, doesn't that stress mechanism that you discovered have to do with the Von Willebrand factor and how that works? Oh, yeah. This is the way I got started. VWF factor, right? Factor VIII. Yeah. This is the way I got started on this. I went to a...

a an anesthesiology conference ted stanley's annuals you know skiing conference this was after i actually retired for about three years because i got so fed up and disgusted with uh the politics of medicine and uh yeah so i invested in trustees and so anyway so i was retired for about three years but then

I made the mistake of fiddling and diddling with the stock market and had two daughters in college. And, you know, so I went back to work. So I thought, well,

I, uh, I'll get some points and I'll go, and I wanted to talk to Ted Stanley about my anesthesia technique, which, so anyway, I go to this conference and the first lecture was by this lady. I've, I've yet to meet her, but my plane was late or, you know, the plane connection couldn't get me to Salt Lake city in time to, to get to the conference to, for that lecture. Got, but I got the book and that evening, uh,

I didn't have anything to do. I was all by myself. I couldn't go skiing because it was dark. So I started reading the book. First, you know, chapter in the book was about recent findings in coagulation. And I found out from reading that, that the vascular endothelium produces von Willebrand factor, which hadn't been known when I was in the, and it releases it into blood in accord with

synthetic nervous activity and that wasn't known when I was in medical school right I see Brad I went to this school that had retained a guy named Rodin who was a Swedish researcher who was very famous and he had been retained by the school to upgrade the curriculum which he did so I got the benefit of his upgraded curriculum you know the biochemistry and everything

And then after we, he deliberately waited, I think, until we had been taught the physical physiology, you know, the basal constriction and the basal dilation, all that stuff. And then he gave us a series of stress theory lectures that just demolished

what we had been taught, what we'd been, we'd passed the test, you know? Jumped through that flaming hulu. And then this was like, we weren't tested on this. He just gave these lectures. He gave these lectures to like 5,500 medical students in his life. And so it was amazing because

I woke up the first time in medical school. I'm in the back row. I'm a rotten student. It's just a big memorization party, which I hate memorizing. It was like a bolt of lightning came out of the cloud. Bam! I sat up and went...

wow, this makes sense. And this is the future of medicine. So I was like a religious conversion. So I always believed that stress theory would one day, you know, be, you know, with what they were missing, as he explained it beautifully. He said, in you, we've got this theory that there's just this one mechanism and everything. But we, we need a testable mechanism.

We've got to have a testable mechanism. And we know what to call it already. It's called a stress mechanism. But we haven't the foggiest idea of what it looks like or where to look. And so what happened was right about that time that I went to medical school, it was being abandoned. For 30 years, it had been the prevailing paradigm of medical research.

But nobody could find any clue of any testable anything that could explain any aspect of Selye's ideas. Hans Selye was the guy who is credited with this theory, stress theory. And so I thought, well, this is fascinating, but I'll never have anything to do with this.

Because, you know, I want to go out and make money, chase women, you know, whatever I'm going to do. But I mean, I always wanted to contribute something to science, but I never dreamed that anything like this would happen to me. There I am, you know, 10, 15 years later, I go to this conference and I get this news and I got so excited.

curious about factor eight now factor eight you know you know a little history about that you guys about do you know the history of factory no definitely not the russian revolution it's it's rolling the russian revolution you're aware of any of that no go for it czar of russia nicholas ii he married one of queen victoria's daughters and they were carriers

of this defect that doesn't affect females, doesn't affect women, but it affects sons. Okay? It's a sex-linked genetic

you know, defect that you inherit. Oh, and the little boy he had was always sick, right? Hemophilia. Yeah. True hemophilia, not Christmas disease, but true hemophilia. Christmas disease is a defect in factor IX, but hemophilia is a defect in the...

male, see the male Y chromosome that determines sex, determines maleness, if you will. It's like missing a leg. So it doesn't have a backup gene. Okay. And so if you get that bad gene, you're in trouble because you don't have, the women have the second leg. They have an X instead of just that Y.

that's lost its tail. Am I making sense for you guys? Anyway, so

This little boy was born, and she had all these miscarriages. But she produced, I think, five daughters, and they were just really, really frustrated because they needed a son to take over. It was probably her body. That was some kind of pushback for having sons. It was doing everything it could to produce daughters because it knew what it had.

Interesting. It could be. I mean, I think that's beyond the scope of my knowledge. That's Steve Scott's knowledge. He knows all about it. Well, all the boy pregnancies would just...

fizzle and die you know they but anyway this one fellow made it he he his name was alexi he ended up getting shot by communists yeah there you go see you do know that word yeah so who who is von willenbrand and what does that have to do with that factor oh well see that's like probably one of the interesting stories that you've told me about is the survivors of the earthquake in japan

and how the sympathetic stress increased their von Willebrand factor and combining with factor VIII and creating a soluble fibrin and blocking up the capillary gates and whatnot. Yeah, von Willebrand factor is a gigantic molecule that's manufactured by the vascular endothelial cells. I mean, now the vascular endothelium is this delicate layer of cells

one cell thick that lines all your blood vessels and it's the sole cellular component of capillaries. These are highly specialized cells and they do several things. Basically from the viewpoint of stress mechanism, there's two main things they do. One is they isolate extravascular tissues from the enzymes in flowing blood.

Specifically, they isolate tissue factor and extravascular tissues from factor VII in flowing blood. Tissue factor, when it gets into flowing blood, it connects to factor VII, which is an enzyme, but it cannot exert its enzymatic properties unless it binds to tissue factor. But when it binds to tissue factor, it becomes activated. Now, same thing with von Willebrand factor. The

vascular endothelium is heavily innervated in your organs, in your chest, in your brain, okay? Your internal organs. Your muscles and peripheral tissues are not innervated with autonomic nerve endings like that, okay? That's just for your internal organs. So in the internal organs,

Synthetic nervous activity stimulates the vascular endothelium to release von Willebrand factor into blood. And the von Willebrand factor is a gigantic molecule which binds to this factor 8C enzyme that's produced by the liver. And it's also a gigantic molecule. So then you have this humongous molecular complex. It's so big that it cannot...

escape blood ordinarily. It cannot pass through the vascular endothelium. So the vascular endothelium is a selectively permeable layer of cell and it allows like various substances to pass back and forth. It allows factor VII, factor X,

and soluble fibrin, which is like a fibular protein, submicroscopic fibular protein, to leak through the vascular endothelium. The vascular endothelium has, you know, the cells have muscle fibers. All eukaryotic cells have muscle fibers, but

inflammation when when you know the stress mechanism generates thrombin which which energizes cellular activity so when the vascular endothelial cells are exposed to thrombin it active it energizes those muscle fibers and they contract and they open up little gaps in between the cells so then your your soluble fibrin can

and your factors 10 and seven can escape through those gaps into the extravascular tissues. And then that you'll, you'll see when you read the book that instrumental in the, the wound healing process, the tissue repair process. Right. So, you know, that's what the stress mechanism, what the stress mechanism does is,

is it regulates hemodynamic physiology. And by doing that, it regulates organ function because organ, you know, blood flow determines organ function. So if obesity is a disease, Brad, how does what he just said connect with what you're looking at at the cellular level for that obesity? Well, it's like I say, I mean, I think these things are all

typically positive feedback loops, right? That there's self-reinforcing systems and, and the, you know, if it is the, if it is the biological imperative of the animal to fatten up, to get through winter, or sometimes this happens there's a, there's a, that's literally a stress mechanism. It's cold. It's winter. Yeah. It's cold. But there's, but there's also a, a hibernating, hibernating,

primate that lives in the tropics that hibernates through the dry season. So it doesn't have to be the fat-tailed dwarf lemur. So it's not always triggered by cold, but drought is another type of stress, of course, and they have their own system to control it. But the point is, yeah, the animal is taking in signals from its environment. Day length,

and all kinds of what types of foods are available. And that's a whole other discussion for another day. But if the animal has decided that something bad is coming, then it's the imperative of that animal to, okay, we better pack on some extra pounds, right? And so these systems, I believe, become self-reinforcing. And what you're saying, the stress is maybe starting to constrict the blood flow. That's causing...

causing these other mechanisms to kick it. That's causing a little bit of a increase in HIF one proteins and they're activating the things that start with glycolytic switch. And then, you know, and like I say, then the, then the fats start to build and that's putting pressure on the blood vessels and it all just kind of snowballs together. And, and you can't really, right. You can't separate the systems. It's all part of one system. It's just, there's intercellular parts and there's extracellular parts and

One of the things that, again, you guys are all young enough to be my kids, you know. I'm like an old fart. So one of the most amazing things for me is that since I finished my training and education and all that, there's been this fantastic increase in knowledge of the capabilities of the eukaryotic cell.

I mean, I've been astonished by this, by the research, like what Brad's talking about here. There's a whole bunch of other stuff like this. These guys beavering away, doing all these elegant studies, you know. Now, I haven't focused on this, but I'm kind of peripherally aware of it. And I'm interested in all of it, but I'm tangled up with this stress mechanism. So I've just focused on that for the last...

Gosh, the book took 20 years to write. This reminds me also, I'm just putting the pieces together, that Ray Peet was against the traditional notion. He thought it was tenuously based in science, the notion that omega-6 and omega-3 are essential fatty acids. And he talks about these studies where they depleted rodents of these molecules and

and they would take these rodents and beat them on the backs of furniture. I don't know what kind of ethics of this study was, but apparently they didn't feel any pain. They didn't feel any pain or anything. It was like the pain was going away, and I thought to myself, well, man, that's interesting. If Lewis Coleman is onto the stress mechanism and Ray Peet was affirmative of that path,

And it's got something to do, I think, maybe with these essential fatty acids to some degree at least because it's interesting how when you depleted them, they did not feel any pain. And they would whack these rodents, grab them by the tail and smack them onto the backs of furniture. Steve, you probably do studies like that with your CO2 tank, but, you know. Well, you're not controlling your variables very well.

well that way i don't know but they did some kind of study there and what if i can jump in here david so this is so this is what you're saying is is precisely correct and the you know the recent series of articles in my blog you know i talk about um these connections right so so inflammatory cells right um

So inflammation is fundamentally anabolic, right? If a macrophage senses that there's an invader, a bacteria or what have you, the macrophage becomes glycolytic.

And it does this even despite the fact that oxygen levels are okay, but it clicks on this process of glycolysis. And it's doing that to create, right, it has to rapidly build. It needs to build membranes to engulf the bacteria. It uses this system where it's producing superoxide, which is a reactive oxygen species. And they have these enzymes on the outside of the macrophages to just blast bacteria

the bacteria with these reactive oxygen species, the superoxide, that's another thing that neutralizes them, but they have to go into this fundamental anabolic state to do this. And if you limit the enzymes that control the desaturases, the delta-6 desaturase and the delta-5 desaturase, what happens is

you get much less of what they call the respiratory burst. You, you, if the cell, because, because the problem, like I said, is that if you're very anabolic and you're doing glycolysis, what you need to do is you need to get rid of the electrons on that NADH, or you can't keep doing glycolysis. And so the linoleic acid is there to remove that NADH, right? And so that, that, that inflammatory process doesn't,

it doesn't go as well or as long if you don't have the linoleic acid to get to continually get rid of that, to get to continually get rid of that NADH. And as I said, then when you look at an active site of inflammation, it very quickly becomes very hypoxic because all of those, because even though the cells are doing glycolysis, which doesn't require oxygen,

You see the amount of those oxidized lipids in that area surge. And to make those oxidized lipids requires a tremendous amount of oxygen, but they're doing it because they need somewhere for those electrons on that NADH to go. And it's driving forward this whole pathway of...

of you know uh we need to get anabolic that means we need to do glycolysis that means we need to ferment these poof uh to remain glycolytic and that gives us this power to build and to spray out you know it enables the cell to survive for a while uh in the absence of oxygen

Right. Or in a hypoxic relative hypoxic state or. Right. But that process, but that process is also driving the hypoxia in that case, because it's because it's taking oxygen. They're using oxygen to ferment those. Just like I say, to ferment that linoleic acid, all of those, um,

pro-inflammatory, if you will, oxidized lipids that you see at the site of the infection. Well, it's getting hypoxic because they're fermenting, right? They're fermenting that PUFA to get rid of the NADH or to remove that, to convert the NADH back to NAD plus. And that allows them to keep doing glycolysis. But that process requires oxygen, right? And they're not burning oxygen in their mitochondria because HIF-1 prevents that and the other things that are activated prevent that.

The reason what's burning the oxygen is the fermentation of these polyunsaturated fats and also the fact that the oxygen molecules are being converted to superoxide by the enzyme systems, right? And so they're flipping the script on oxygen usage. And one of the ways that they do that is by fermenting linoleic and linoleic acid together.

Which, of course, is being steadily replenished as free fatty acids as they fight this battle. They're pulling the glucose and they're pulling the PUFA from the bloodstream to continue this process of glycolysis. This is all relevant. I want to just pitch this at you as a spitball on the side because there's the...

oh shoot what about blanking the um the cambrian yeah explosion yeah yes and of course everybody has heard of that um well you know they've discovered these uh organisms thriving you know hundreds of them and every time they go down to in the in these deep dive contraptions um

the ones that work and don't kill everybody anyway, and these volcanic rift zones, and they're finding all these tube worms and what looks like crabs and fish and clams, you name it. I mean, this is like hundreds of different organisms, and the microbes are so thick.

that they cover the rocks. I mean, it's just like a layer of both eukaryotic cells and bacteria and I'm sure archaea. And they're just all... They're eating these toxic volcanic chemicals that are just flowing up out of there, okay, in these rift zones that ring the earth like the seams of a baseball. And so these things look like familiar creatures, right?

But they're using different metabolic pathways, completely different from your land-based terrestrial or even ocean-going marine creatures and single-celled creatures as well as multicellular creatures that we're familiar with, right? This has just been discovered very recently. Yeah.

Yeah, you know what I'm talking about. To put that into perspective,

If you believe the latest, earliest animal fossils or potential animal fossils that have been found are about 900 million years ago. What looks like the material of sponges in, you know, they're not very well preserved. You can't tell that it's a sponge, but you're like, where else did this fiber come that's in this rock if it's not from a sponge? Right. And so that's, so we could, I think we can say that

That animal life started around a billion years ago. And remember that back then there was much, much, much less oxygen in the oceans than there are today. And so that first, you know, the first the hundreds of millions of years before the Cambrian explosion happened in.

an environment that's much lower in oxygen than the environment that we have today. My supposition being that those strange looking things living down deep in these thermal beds and low oxygen areas probably have been that way the whole time. And in the rest of the ocean, the oxygen levels increased and then on the land, the oxygen levels increased and we've moved around. But

This is another thing I talk about on the latest blog. So I have a post called pregnancy is hypoxic. And so,

That's true. Yeah, that's true. If you look in the oxygen pressure in the body is similar to... I'm pretty sure it's similar to the deep ocean or 5%. I don't know exactly where that happens in the ocean, but it's a more primordial state, the low oxygen state. And that's how, of course, all cells evolved. The cells evolved in the absence of oxygen. And then later, oxygen came and

Um, and the cells use that to their advantage. Ultimately, uh, at first it was probably very bad for most of them, but ultimately some learned how to use it as a tool. Right. Um, and so when a, uh, when, when I, an egg is fertilized, um, one of the first things that happened within the first couple of days is in the mother, the, um, the artery that feeds into the uterus is blocked.

And so the partial pressure of oxygen, it becomes quite hypoxic. And I'm arguing that that hypoxia favors a glycolytic state, a glycolytic, very anabolic state. And in those first weeks of pregnancy, those cells are rapidly dividing. And that's what you see in anabolic cells. The cancer cells are glycolytic and they're rapidly growing. The immune cells are glycolytic and they're very anabolic.

the obese, um, the, the adipose tissues in the obese are glycolytic and therefore presumably anabolic. And that's probably why the fat cells are growing, right? That, that is the fundamental, uh, growth. The anabolic state is, is hypoxia. And so the mother wants that, um,

You know, wants the the the egg to grow the fetus to grow and so she restricts oxygen to keep it in a replicate a replicative state and and in the early embryo, almost all of the cells are still some cells they're all all able to grow and and divide and then

As the baby comes closer to term, more and more oxygen can reenter the placenta. So over time, the oxygen levels get higher and higher. And what does that do? That stimulates...

mitochondrial growth that stimulates the production of reactive oxygen species in the in in the cells and those reactive oxygen species become the signal to the cells that okay we don't need to be stem cells anymore we can differentiate and we can become grown-up adult cells because oxygen is here and now we're sensing the oxygen via these ROS

uh, you know, sensing molecules. And now we can become adult differentiated cells that are no longer just growing and reproducing. Yeah. I'm curious, I'm curious about what, what exactly is your research specialty? Uh, well, I, you know, um, so I'm developed right now. I'm working on a, um, a cell culture, I would say. So right now I'm working on a cell culture, um,

assay that is going to look fundamentally at how changes in the environment, meaning

In this case, it's the cell culture medium, but of course that's supposed to represent the serum of the blood, right? When you change that, how does it affect the NADPH and the NADH and the ROS levels in the cell and whether they're more likely to store lipids or give off lipids? And how does that process look? And so I'm sort of in the process of developing that whole thing, but that's my big research area.

project that I've been chatting with David about this too. So this is going to be very right. So now we finally live in an era where we have, they have robots that do the pipetting.

I have a very powerful microscope that can image 384 well plates. So you have 384 little experiments in a plate this big. And then we can start to use AI to build models about what's happening and what's essentially controlling the flow of electrons through the cells.

um the the theme of the lab is follow the electrons um so that's that's kind of what i'm working on and uh yeah that's that's where my brain is these days i've done other things i've jumped around i was i was out of science for a little while i actually started a uh a local meats butcher shop and uh uh pastured pork uh farm so i'm how'd you get out of it and get back into it

Uh, well, it's been a journey. People who, like, so I, you know, essentially, I've

Long story short, that business just wasn't financially successful. They left. That's when I started writing and the blog took off and I've been able to get work in the lab. And I've been able to, you know, mostly through my supplement sales, I've been able to get a little bit of an egg together that I've been able to purchase some of this equipment. And now we're in the kind of starting to get into the fundraising stages. Are you...

University or something? You must be. No, I'm at a funky old lab building in Buffalo, New York. And it's great. It's inexpensive space and it's legitimate lab space. It's a little out of date, but that's okay. We can live with that.

I kind of like it. I like it. It's kind of retro. Yeah. I mean, you can see these little bookshelves. They're great. I want to ask Steve to kind of help with the bigger picture for the audience. You know, we've got a few things here. You know, Brad's saying that, like, you know, this is a hypoxic state that this obesity disease is in, and it's similar to how the pregnant mother creates a hypoxic state to create growth rapidly, right?

And then we think about obesity and its association with cancer, right, which also has to do with hypoxia. We see how it's related to these similar diseases that all kind of come about from this stress mechanism. So we're putting all the pieces together. You know, how does your understanding of oxygen and carbon dioxide and maybe some of the applications and things that you've looked at for humans, how would those work?

come in play to help us understand how to heal or treat this problem of obesity and cancer and all the related diseases that seem to be kind of stemming from this same problem? Yeah, that's a good question. A lot of this... Yeah, go ahead. Yeah, a lot of this stuff that I'm hearing from Brad is very new to me, so I don't know. I'd have to read more of his blog posts to really like see how CO2 would play a role. I know that transdermal CO2 or injecting CO2 into fatty tissues seems to

Increase the metabolism and burn off fat. I know CO2 will help increase angiogenesis and increase blood flow to the hypoxic fat tissues and increase...

capillary density within those tissues and potentially help. One moment. Brad, you said that it's a pseudo hypoxia that obesity cells might have because the oxygen's there, but it's not able to be used. What you just said about oxygen going to the

tissues of fat cells because of CO2. Does that overcome that or no? Anybody know here? I'm just wondering. Well, my, my understanding, what Steve's talking about is, is the idea that the CO2 injected into the, into the fat tissue is allowing essentially more oxygen to get into the tissue because it's the mechanism that was pointed out of the, the CO2 competing with the hemoglobin to deliver more

oxygen to that tissue. I believe that's correct, Steve. And if so, I think this, that was my understanding. I thought we were, if that's the case, then

we are sort of largely in agreement, but I don't know. Steve can tell us if that's what... Yeah, that's my understanding of it too. I just don't know if that theory fits within what you're talking about. I need to do more research on what you're looking into. Steve, what about the... Well, first of all, I remember you told me about your girlfriend who got

I'm enthusiastic about spending a lot of time inside your CO2 suits and she melted the fat off her backside. Remember that? Yeah, reduced her cellulite and helped reduce fat just being in the suit for hours at a time. Is cellulite the same as obesity here, Brad, or no? Is that the same thing? I'm not sure what...

Yeah. I've never quite understood the meaning of that word, to be honest with you. What, cellulite? Cellulite, yeah. Well, it's kind of lumpy fat on your... Yeah, if you look at the old paintings, people didn't have, when they were obese, they didn't have cellulite as much, it seems like. Right. And some people have suggested it's because of the introduction of these seed oil foods.

Right. Sure. Sure. Yeah. And I mean, again, if, if that's, if the, if the CO2 is, is diffusing into the skin and that's allowing more, you know, oxygen delivery to those tissues, that's exactly what I would expect. You know, I think that the one thing, so one of the, I think one of the reasons is that I'm, I like biology and then I'm, I think I'm pretty good at it is I,

I'm sort of comfortable not assigning absolutes to anything and that everything is sort of like biology is generally counterintuitive. It's often not what you think on the first glance. It's, it tricks you and it's, you say, oh, well, you know, just because the, the, the obese cells are now, you know, glycolytic and, and, and because that process of limiting oxygen,

in some contexts, cause the growth of blood cells does not mean that the now hypoxic

um adipose tissue is now fully you know uh vascularized it doesn't because it depends because it depends on the context all of these mechanisms are context dependent you have to think about the individual tissue and the individual case and what happened earlier and what happened now that the obesity has developed and what was the beginning and what was the end and what you know so you can't there's no absolutes here but i'm assuming these obesity cells are more um

Normally the pH gradient in cells and external environment of the cell that's a little more acidic inside of the cell and more alkaline and outside of the cell. But I'm assuming in this obesity situation or diabetes, I know in diabetes for sure that the pH gradient is somewhat reversed or the gradient is less. So the inside of the cell is more alkaline and the outside is more acidic. And that might just the external environment of the cell being acidic and have a lot of like...

lactate might um exasperate the situation making a more glycolytic um situation the co2 might help reverse help reverse that ph gradient potentially and it slightly acidifies the cells the proteins in the cells and helping to structure the water and whatnot and yeah that's interesting because yeah i mean the the the uh

the obese glycolytic cells are definitely giving off more lactic acid. That's, that's what you do. That's what you do in glycolysis. And there's evidence that as, as capillary blood flow goes through a, a adipose cell bed in obesity, that lactic acid does indeed increase across that capillary bed. And I think in the obese environment and the, there's less, um,

removal of the waste products too. There's less like lymphatic drainage. There's less like venous return, less blood flow. So things, these toxins, well, lactate is not a toxin, but these byproducts of metabolism, they tend to accumulate in the environment. And I think potentially breathing CO2, it kind of, it makes you breathe faster. So you're creating like this

thoracic pump almost like when you're exhaling, you're it's creating this positive pressure. And when you're inhaling and creating this negative pressure and it's kind of drawing the lymphatics up and then pushing, uh, it's kind of like its own heartbeat in a, in a sense, it's creates its own, own wave. They call it a Vassava wave and it might help.

push, create a better environment inside the fatty tissue where you're getting more tissue perfusion and getting more waste products removed through breathing CO2 potentially because of the, of the deeper breathing and you're, you're opening up everything and getting more blood flow in there. And maybe my, my idea is, um, that potentially that the fatty tissue is, um,

it's kind of stagnant. A lot of those things tend to accumulate. Steve, tell them about the bats and the mole rats. Yeah, I mean, the mole rats and the... They basically... Naked mole rats, they generally live like an average of 34 years, where a rodent the same size normally lives like one and a half to two years, maybe three years at the most. And they live in very high CO2 environments, and they...

They never get cancer. They basically don't age. They don't die of old age. They die of a predator or something like that. They're hypoxic, too. Yeah, they're also hypoxic, too. How can you be hypoxic but yet not obesogenic or cancerous like the naked moran? This has been a super enlightening episode. Sure, you can be... It's sort of like Lewis was describing before. We're looking at

We're looking at a photograph when what's actually happening is a video is playing, right? And so you look and you say, well, it looks hypoxic, but that might be because it has increased oxygen delivery to the tissues is why the blood looks hypoxic because the oxygen is being directed into the tissues rather than hanging out in the blood.

Right. And so is that what's going on with the baby in the womb is more oxygen getting into the cells because of my misunderstanding? Well, not necessarily. Right. No, the opposite is happening. Right. So what I'm saying is that there's two. Right. So. So in the womb, in the mole rat, if you look in the blood, it's hypoxic because the blood is circulating like the mole rats breathing. And as Lewis pointed out, it's probably being saturated in the lungs, even in a burrow and a high CO2 environment. But

But if it's high CO2, then oxygen delivery to the tissues is actually increased, right? So you have more oxygen flow to the tissues. Whereas in the hypoxia, and that causes the mole rat to be...

young perhaps, but adult, right? It causes differentiated cells. It causes, you know, an adult mature organism. Whereas in the baby, the mother is restricting all oxygen flow. And so that's true hypoxia, right? Like that's hypoxic because the oxygen is limited as opposed to, as opposed to hypoxic because oxygen delivery to tissues is increased. How can we all be more like naked mole rats where we can live forever with no diseases?

I, I, I, I'm going to do an experiment on myself. I, I've been meaning to, to send it. You know, I've got a pro or a natural gas burner that's designed to go in a greenhouse and it's all set up to work during daylight, unfortunately, because what I wanted to do is it is I'm going to mount it in my bedroom.

And I've got a ceiling fan in there. And so at night, I'm going to close myself in with a cat.

Don't try this at home, folks. Whatever he's about to say next. You know, guys have been doing experiments on themselves since forever, and so that's what I'm doing. I'm not doing this to anybody else. But, I mean, people have, I mean, they can't, the big pharma can't stop you from doing this as an individual, right? Yeah.

Yeah. But but anyway, I found this system that's all set up. And I don't want to use it in the summer in Bakersfield because, you know, just going to jam my air conditioning bill sky high. But in the winter, it'll it'll heat the bedroom and it'll heat the house. And what is this? What is this system? Yeah.

Well, it's like a natural gas burner that, of course, when it burns natural gas, and as it does so, it generates carbon dioxide. And it's designed for use in a greenhouse for seedlings and things. You know, it doesn't take very much, just a little bit of elevation of your CO2 partial pressure. Because CO2 in the ambient air is a trace gas, even at sea level.

it's only 0.03% of the atmospheric gas mixture. And that's not very much. And most of that hovers right at the surface of the earth. And it's, in other words, it's being produced by volcanic or bacteria way deep beneath the surface of the earth. And it, and it's constantly seeping up to the surface and that's where we get our CO2. And, um, so, um,

Well, it's a very tiny elevation of the concentration of CO2. I'll never forget my botany professor at Ohio State mentioned that here in the Central Valley of California, where I'm living now, back then I was at Ohio State, you know, he mentioned this is the most productive agricultural land in the world. Wow.

But why is that? It's because it's surrounded by mountains. It's kind of a bowl, if you will, a valley surrounded by mountains. And the mountains trap carbon dioxide. And so it's just a little bit higher concentration of carbon dioxide here in this central valley of California.

So everything grows, you know, the cotton grows taller and faster and the fruits and everything. This is the most productive farmland in the world.

And I never forgot that. That was a practical tip, you know. Another idea you could do is if you could sleep in a tent on your bed. Yeah, you could. It would accumulate the CO2 that you breathe off to some degree. Yeah. Brad, how does that fit in with what you've studied with every little animal known to man, these copalods and copalods and all the things that the Japanese eat?

Yeah, you know, let's remember that when life crawled out of the ocean, I don't know the exact numbers off the top of my head, but oxygen levels were

were lower than they are now and co2 levels were uh presumably higher than they are now oh yeah they were way higher way way that's true right and so so the the first um you know amphibians would have been uh that adapted to you know life out of the water uh would have been in a high co2 lower much lower oxygen environment and so that's so life is not um

You know, all this other stuff is this higher oxygen, lower CO2 level is much newer. But it looks like there's some kind of thing in the future that we can understand. We have to get these diseases under control. People can't think straight. And if you can't think straight, you can't act straight. You can't do good things for people. You know what I mean? So it all comes together. That's why I have Steve Scott on here. He's trying to help people.

Anything else you wanted to add before we land the plane here and get some more CO2? Yeah, just real quick. This fits into my unified theory of biology, but my understanding is that most of the oxygen we breathe is

comes from photosynthetic bacteria, not from leafy plants in the Amazon. You know, everybody gets their panties in a wad because they're burning down the trees in the Amazon and everything. Oh my God, we're all going to die of oxygen starvation because of these guys. No, you know, the vast majority of the oxygen is coming from photosynthetic bacteria that are ubiquitous on the surface of the earth and in the water too, you know?

But they take sunlight and combine it with carbon dioxide, and they produce oxygen as a byproduct. The cyanobacteria caused the oxygen catastrophe. In the early days, the cyanobacteria were photosynthesizing, releasing oxygen, and most...

life on earth perished because of the rising oxygen levels and it hadn't dealt with it yet and then eventually yeah right things dealt with it and life went on yeah it caused a conversion to a new type of life forms you know yeah i don't have all the answers by any means but this is fascinating stuff and one thing i wanted to to draw your attention to i don't have the answer to this but

the eukaryotic cells in these animals that live in the RIF zones, they couldn't use the Krebs cycle because that's a hypoxic environment. So they're using different metabolic pathways to generate ATP. Now, what I think happened is that

All these different anatomical forms developed in these rift zones over millions and billions of years. You know, the fish forms and the crayfish and the tube worms and clams and you name it. I mean, I don't know. There are three, four hundred of them that have been identified so far, you know. And they look just like the stuff we're familiar with. But...

you know, you bring them up to the surface, they're instantly dead. They, you know, they can't use oxygen. They use the toxic volcanic chemicals. And I did find a study, I blundered into a study. I don't know whether Steve sent it to me or Jeff Walden sends things to me like Steve does. And apparently the eukaryotic, they found these eukaryotic cells that, that, you know,

sounded like they had engulfed some other type of organisms with the ability to metabolize volcanic chemicals or something. I don't know. But, you know, the theory as I understand it today is that the eukaryotic cell is sort of a predator cell and that it has engulfed

previously free-living bacterial cells. And some of those have

achieved a sort of symbiotic state within the eukaryotic cells and the mitochondria are an example of that. So mitochondria have their own DNA and RNA and everything, but that's isolated from the nucleus by the thick walls of the nucleus. And I think that's to prevent contamination of the two different types of DNA.

Yeah. So the eukaryotic cell can engulf things and sometimes they survive inside there. And, and then over time they, they lose a lot of their anatomical characteristics and, but they, it's like a symbiotic relationship, you know? Yeah.

the mitochondria is doing something for the eukaryotic cell, enabling it. So what I'm hypothesizing here, and this is not in the book, okay? I'm trying to tell you that when you read the book, my thinking hadn't advanced to this point. I wondered how this happened because obviously if...

life progresses by evolving new stress mechanisms that adapt to unique sets of environmental circumstances and that that's the theory right right uh then the cells um you know they have to um

you have an extra, you have interest, interest, cellular stress mechanisms. In other words, each cell has a, a stress mechanism within itself that may structure and, uh, you know, works as metabolic activity and, um, keeps it alive. Okay. But then I'm talking about an extra cellular stress mechanism that, uh,

you know, is operating outside the cells, but providing the cells with ATP and creating an internal environment in the animal or plant that facilitates the growth and survival and activity of the cells, right? They have to have oxygen, they have to have food substances, they have to be maintained in a certain, within certain temperature ranges,

you know, and things like this. And, you know, of course, acids and bases and all that. So the stress mechanism, this extracellular stress mechanism is maintaining ourselves in a happy environment. Well, when there has to have been a new type of eukaryotic cell that can utilize oxygen that enabled

to the Cambrian explosion because here you have all these animals animal forms living in the rift zones eating these you know thriving on the volcanic chemicals which are very energetic I think ATP is you know like a holdover a remnant it's still used as like a universal medium of energy exchange

And that's what is you guys, you're the biologists, phylogeny recontribulates ontogeny and all that. Nature is conservative. It keeps on using the same things as long as they're working. Absolutely, 100%. So there must have been a seminal event where somehow

These eukaryotic cells that were thriving in the rift zone suddenly gained the ability to survive with oxygen instead of toxic volcanic chemicals. Yeah, I think that's probably exactly right. Yeah, but their DNA had somehow retained oxygen.

all these anatomical shapes and ability to change their sizes and everything. And so one of the things that I believe from my reading is that we have, each of our cells has all these different genetic blueprints and

you know, anatomical shapes and metabolic pathways are, they're inactivated or quiescent and they can be reactivated under severe extreme circumstances. And, you know, the sex mechanism keeps capturing

you know, mutations and culling the ones that are destructive and harmful and retaining the ones that might be useful at some point in the future that they're at least not causing any harm. And once in a while, you know, it's got something that can be really useful under, you know, under certain circumstances. So, you know, when you have these dramatic changes,

environmental changes like the earth has gone through some pretty dramatic changes so for the zillions of years that it's been around and

I want to shut up at this point because I don't want to spoil Brad's fun when he reads my chapter. I want to see what your reaction is when you get there. Just understand that since I wrote that and published it, I've gone on and I've developed some... That was one example I just want you to be aware of. We're getting close to the point where

If my book ever starts selling and getting, you know, appreciated for what I think it is, I think this book is going to be one day regarded as the principia of medicine. You know, the most important advance in medical theory in the entire history of recorded history, you know, of medicine. Yeah.

And it's going to reform and revolutionize medicine, make it much simpler to treat cancer and, you know, crisis and critical illnesses. Right now, it could revolutionize medicine right now, just with our present technology.

medications, machines. I want to land the plane here. Steve or Brad, do you have any final thoughts or questions or anybody have any questions for each other? My only statement is hopefully, I don't know exactly when this video comes out, but the article that I mentioned about the polyunsaturated fat,

Wasting All Your Oxygen should be live on fireinabottle.net near the top of the thing when this comes out, so go check it out. Yeah, this is a great talk. I learned a lot about – I've known Lewis Coleman for a long time and studied his work, and a lot of the things that Brad talked about today was really new to me, so I'm really excited to read his blog posts and the new ones that he's coming out with.

Yeah, we need to exchange our email addresses. Yeah. I could do these kind of conversations for all day, hours and hours, but we've got to get out in the sun and we've got to get our CO2 retention and everything else, right? Yes. Absolutely. Brad, you're about to bust out that window. I can see all the energy you have. I am. I'm like, it's hard for me to sit still this long. Yeah. You've got more energy than a whistle pig for sure, don't you? It is.

I appreciate you guys coming on, guys. FireInABottle.net for Brad's blog series. We've got Stress.org where you can learn about the American Institute of Stress where Dr. Lewis Coleman is their chief scientist. I'm sure that's a very stress-free work environment there, right? Yeah, one other little plug. Dan Kirsch, who runs the American Institute of Stress at this point, has financed a movie.

that just got completed a couple of weeks ago. And I can't, he made me swear to God, I wouldn't share it with anybody because I would love to give you the link for it. But he's, I think he wants to see if he can win some awards to draw more attention to it. Yeah.

And so he's working on that. So he made me swear I wouldn't share the video link, unless you want to come here and visit me in Bakersfield, which is about the only thing worth seeing or doing in Bakersfield. But as soon as the movie becomes available, I'll certainly share it with all you guys. And Steve, what do you want people to leave with?

Yeah, that carbon dioxide is not a waste gas. If you think about it, we don't store any oxygen in our body, even though it's essential. And we would die without it within minutes, yet we don't store any because it's very reactive. And CO2 is, we actually retain CO2, we actually blow off all the oxygen that we don't use. And CO2 is the good guy, and oxygen is more of a toxin, more reactive than oxygen.

Then even carbon dioxide, because we store carbon dioxide in oxygen and we don't. And CO2 is necessary for oxygen to be delivered to the cells. Kind of like the protective wings around oxygen to help deliver it and also protect you from the overproduction of the reactive oxygen species and whatnot. David, we could do a whole one of your shows just on the anesthesia hoax that vilifies carbon dioxide as toxic waste like urine.

And there's also, I think, DuPont is a major player in maintaining this nonsense about carbon dioxide. Trump signed an executive order that says that carbon dioxide is harmless and useful and everything. Of course, he's thinking about encouraging oil production. And just be careful about injecting it in certain places. We don't want to get anybody harmed. Yeah.

Yeah. Also, I've been working on a book about CO2, working on it for the last year and a half, and you'll be able to get it from Carbogenetics.com. Yeah, I want to give a shout out to Carbogenetics because I've used their inhalation and their bodysuit, and it's a lot of fun. When I get in the bodysuit, I look like the girl from Willy Wonka after she's been buried in Canada. Yeah.

That's why I like to take photos and say, hey, look, this is how good this sugar diet is doing for me. See? And I send photos. Yeah, but when you get out of it, you look a lot better. You look like Superman or something. Oh, yeah. And look at that skin I got. Look at that. You wouldn't believe I'm 57. Can you believe it? Yeah.

All right. You take care, guys. I appreciate your time. Remember, you can email us hello at the neighbors choice dot com. Leave a comment or question you have in whatever facility that you're watching this program, whether it's a social media video platform or audio platform. We'd love to hear from you. And this is what we do here, folks.

Many people have told us that we're like academia in exile. We don't have the full facilities and the funding, but we have this network of people, unlike anything in the world, where we can bring together a Manhattan Project for Cancer, which is something I've been doing with a whole host of people, or we do something like this where we fascinate people

have all these fascinating conversations about oxygen and its role in relationship to CO2 and obesity and everything else. This is cutting-edge stuff, folks. I appreciate your time, and thank you all for participating in it. The world is a man to pass his time. If not himself, there's not to say the words to his end of the world.

I took the toll.